Terminal differentiation of human granulosa cells as luteinization is reversed by activin-A through silencing of Jnk pathway.

ABSTRACT: Molecular mechanisms underlying luteinization (terminal differentiation of granulosa and theca cells after ovulation) and luteolysis (demise of corpus luteum) are poorly understood in human ovary. Here we report that activin-A, after binding to its cognate receptors induces a functional luteolytic state and reverses luteinization phenotype by downregulating the expression of the steroidogenic enzymes, LH receptor and VEGF and reducing estradiol (E₂) progesterone (P₄) production and upregulating FSH receptor and cyclin D1 expression in human primary luteinized granulosa cells. Further, this action of activin-A involves downregulation of JNK signaling pathway and is opposite to that of human chorionic gonadotropin (hCG), which acts as a luteotropic hormone and improves

SUBMITTER: Bildik G 

PROVIDER: S-EPMC7511402 | biostudies-literature | 2020

REPOSITORIES: biostudies-literature